Morphine-potentiated cognitive deficits correlate to suppressed hippocampal iNOS RNA expression and an absent type 1 interferon response in LP-BM5 murine AIDS

J Neuroimmunol. 2018 Jun 15:319:117-129. doi: 10.1016/j.jneuroim.2018.02.017. Epub 2018 Mar 6.

Abstract

Opioid use accelerates neurocognitive impairment in HIV/AIDS patients. We assessed the effect of chronic morphine treatment and LP-BM5/murine AIDS (MAIDS) infection on cognition, cytokine production, and type 1 interferon (IFN) expression in the murine CNS. Morphine treatment decreased expression of pro-inflammatory factors (CCL5, iNOS) and reduced cognitive performance in LP-BM5-infected mice, correlating to increased hippocampal viral load and a blunted type 1 IFN response. In the striatum, morphine reduced viral load while increasing IFN-α RNA expression. Our results suggest that differentially regulated type 1 IFN responses may contribute to distinct regional outcomes in the hippocampus and striatum in LP-BM5/MAIDS.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • AIDS Dementia Complex / immunology*
  • Analgesics, Opioid / toxicity*
  • Animals
  • Cognitive Dysfunction / etiology
  • Hippocampus / drug effects*
  • Hippocampus / immunology*
  • Hippocampus / virology
  • Interferon Type I / immunology
  • Interferon Type I / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Morphine / toxicity*
  • Murine Acquired Immunodeficiency Syndrome / immunology
  • Nitric Oxide Synthase Type II / biosynthesis
  • Nitric Oxide Synthase Type II / immunology
  • Viral Load

Substances

  • Analgesics, Opioid
  • Interferon Type I
  • Morphine
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse